Oral Cavity, Mucosal Disease and SCC of the Head and Neck

Masses displace the parapharyngeal fat posterolaterally, styloid muscles posteriorly.

Pharyngael Mucosal Space

Airway side of pharyngobasilar fascia (superior aponeurosis of superior pharyngeal constrictor, inserting into skull base). Contains upper aerodigestive tract mucosa (squamous and ciliated columnar epithelium, submucosal lymphatics, minor salivary glands), posterior 1/3 tongue, lymphoid tissue (adenoids, lingual tonsils). Easily assesed by clinician. Mucosal/adenoidal hypertrophy and prominent nodes are common after URTI, unlikely sinister unless there is assymetry, invasion of fascial planes or associated adenopathy. Nasopharynx (posterior to choanae), oropharynx and hypopharynx. Subsites include piriform recesses (edges of the ‘flying saucer’), posterior pharyngeal wall, postcricoid region. Lesions include NPC, SCC, lymphoma, minor salivary gland tumours, juvenile angiofibroma, rhabdomyosarcoma.

Lingual Thyroid

Arrested descent from foramen cecum at junction of circumvallate papillae. Typically midline, hyperdense, enhancing. In 80% this is the only functional thyroid tissue; in other cases may have tissue in neck. Incomplete descent of thyroid gland is uncommon.

Pharyngitis and Tonsillitis

Pharyngitis and tonsillitis usually spread from viral rhinitis. May have bacterial superinfection esp β-haemolytic strep, S.aureus. Nasopharynx may be covered by exudative pseudomembrane. Enlarged erythematous tonsils (reactive lymphoid hyperplasia) with exudate emanating from the tonsillar crypts (follicular tonsillitis).

Tonsillar abscess – Hypodense with peripheral enhancement, adjacent fat stranding, high T2. From Strep.pneumoniae, Strep/viridans, often multiorganism. Most commonly peritonsillar and retropharyngeal. Pharyngitis and retropharyngitis may cause Grisel syndrome (torticollis with rotatory subluxation of C1 on C2). Necrotising adenitis is paramedian along retropharyngeal nodes; abscess if crosses midline.

Croup

See Paediatric Chest

Supraglottitis

See Paediatric Chest

In adults supraglottitis usually from streptococcus with milder infection. Uncommon acute respiratory obstruction. Enlarged epiglottis, aryepiglottic folds and arytenoids. Width of epiglottis:C4 is >0.33, prevertebral soft tissue:C4 >0.5, hypopharyngeal airway:C4 >1.5.

Obstructive Sleep Apnea (OSA)

Narrowing of airway from fat, redundant mucosal and muscular tissue, hypertorphy of lymphoid tissue. Reduced cros-sectional area of oropharynx at soft palate, base of tongue or uvula levels <50mm2 (normally 100mm2).

Pharyngeal Zenker’s Diverticulum

  • Zenker’s diverticulum – Dysphagia, halitosis, aspiration pneumonia, regurgitation of food. Posterior outpouching at Killian’s dehiscence (relative weakness between cricopharyngeus and inferior pharyngeal contstrictors).
  • Killian-Jamieson lateral pharyngooesophageal diverticulum – Usually smaller, protruding laterally.

Thornwaldt Cyst

(Tornwaldt cyst). Aberrant remnants of notochord in midline nasopharynx, in 1-2% of population. Hypodense, usually bright T1 and T2 (contains protein). May become infected.

Mucus Retention Cysts

Obstructed minor salivary glands, may be from previous infection, anywhere in head and neck mucosa. Commonly around fossa of Rosenmuller. Round, well-defined, low T1, high T2. DDx Thornwaldt cyst.

Inclusion Cysts

Epidermoid and dermoid cysts may occur in the tongue or floor of mouth. Geometric shape.

Vascular Malformations

  • Venous vascular malformations – Common in tongue. Usually hypperdense, avid enhancemnt, may contain phleboliths.
  • Capillary haemangioma – Subglottic narrowing in an infant (DDx idiopathic subglottic stenosis). Usually 1-2yo. 50% have cutaneous haemangiomas. Asymmetric narrowing of subglottic airway, smooth enhancing mass. In adults haemangiomas usually supraglottic. Regresses spontaneously, with beta-blockers, steroids or laser.

Neurogenic Tumours

Schwannoma or neurofibroma. Exophytic or submucosal iso T2 enhancing masses involving hypoglossal, lingual or superior laryngeal nerves (esp aryepiglottic fold). May have atrophy of innervated muscles.

Minor Salivary Gland Tumours

Minor salivary glands along aerodigestive system, esp soft palate.

  • Pleomorphic Adenoma (50%, benign mixed tumour) – Round, well-defined, very high T2, enhances.
  • Malignant tumours (50%)
    • Adenoid Cystic Carcinoma – Indistinguishable from SCC. Propensity for perineural spread (in 60%), with rapid extension into noncontiguous spaces eg orbit via inferior orbital foramen, cavernous sinus via foramen rotundum (and brainstem via trigeminal nerve), infratemporal fossa via pterygomaxillary fissure.
    • Mucoepidermoid carcinoma
    • Acinic cell carcinoma
    • Adenocarcinoma
    • Pleomorphic low-grade adenocarcinoma
    • Undifferentiated carcinoma

Non-Hodgkin Lymphoma (NHL)

Indistinguishable from SCC. Usually associated with other nodal and extralymphatic involvement eg splenomegaly.

Oral Cavity and Dental

The tooth crown is covered by acellular enamel, dentin (contains odontoblasts) and pulp chamber (loose connective tissue with nerves, lymphatics, capillaries). Dentin extends down into alveolar bone as roots, lined by cementum and attached via the strong but flexible periodontal ligament. Gingiva is the squamous mucosa between and around teeth.

Macroglossia from acute allergy, hypothyroidism, amyloidosis, Down syndrome, glycogen storage disease, mucopolysaccaridoses, NF, idiopathic/familial macroglossia, Beckwith-Weidemann syndrome, acromegaly, lingual thyroid, haemangioma/venous vascular malformation.

Caries

(Tooth decay). Mineral dissolution by acid end-products from bacteria capable of fermenting sugars (Strep.mutans and Lactobacillus). Fluoride incorporates into enamel (forming fluoroapatite), contributing resistance to degradation. Dental plaque is a biofilm on the tooth; if persists becomes mineralised to form tartar (calculus). Bacteria in the plaque erodes the underlying enamel.

Gingivitis

Inflammation of gingiva, usually from poor oral hygiene, plaque build-up beneath the gumline. Chronic gingivitis causes erythema, bleeding.

Periodontitis

Inflammation involving the periodontal ligaments, alveolar bone, cementum. Thought to be independent of gingivitis, ?shift in type and proportion of bacteria along gingiva. Occasionally associated with AIDS, leukemia, Crohn, diabetes, Down syndrome, sarcoidosis. When severe there is destruction of the ligament and loss of alveolar bone. May cause infective endocarditits, pulmonary/brain abscesses, adverse pregnancy outcomes.

Inflammatory/Reactive Mucosal Lesions

Fibrous proliferative lesions:

  • ‘Irritation’ fibroma – Buccal mucosa along bite line, or gingivodental margin.
  • Peripheral ossifying fibroma – ?Maturation of a pyogenic granuloma of the gingiva. Similar to pyogenic granulomas.
  • Pyogenic granuloma – Vascular, ulcerated, may have rapid growth. ?Form of capillary haemangioma. More common in children, young adults, pregnant women.
  • Peripheral giant-cell granuloma – Aggregations of giant cells. Similar to pyogenic granulomas.

Aphthous ulcer (canker sore) – Single/multiple, shallow hyperaemic ulcers. Resolve in days to weeks. Unknown cause. Recurrent in caeliac disease, IBD.

Glossitis – Beefy red tongue from certain deficiencys with atrophy of papillae exposing underlying vasculature. May also occur with jagged carious teeth, ill-fitting dentures.

Infections

  • Herpes simplex – Most HSV-1, occasionally HSV-2. Acute herpetic gingostomitis with vesicles and ulcerations.
  • Other viruses – Herpes zoster, EBV, CMV, enterovirus (hand-foot-mouth disease), rubeola.
  • Oral candidiasis (thrush) – Pseudomembranous, superficial grey-white inflammatory membrane.

Hairy leukoplia – Immunocompromised, seen in 80% of those with HIV. White confluent patches of fluffy/hairy hyperkeratotic lesions esp lateral border of tongue which cannot be scraped off (cf thrush). Probably caused by EBV.

Odontogenic Cysts

Inflammatory cysts:

  • Periapical/radicular cyst/abscess – Long-standing pulpitis (from advanced caries or trauma) -> necrosis into alveolar bone. Over time fills with granulation tissue, forming a periapical granuloma.
  • Less common:
    • Residual cyst
    • Paradental cyst

Developmental cysts (most), from remnants of odontogenic epithelium.

  • Dentigerous cyst – Around crown of unerupted tooth, usually mandibular 3rd molar. ?Result of degeneration of the dental follicle. Unilocular lytic expansile with sclerotic margins adjacent to the unerupted tooth, spares cortex. Incomplete excision may result in recurrence, rarely transformation into ameloblastoma or SCC.
  • Odontogenic keratocyst (OKC, primordial cyst) – Locally aggressive, 10-40yo, M>F, posterior mandible. If multiple, may be associated with basal cell nevus syndrome. Unilocular or multilocular, expansile, erodes cortex but doesn’t perforate it. Recurrence if now completely removed in 60%.
  • Less common:
    • Gingival cyst
    • Eruption cyst
    • Lateral periodontal cyst
    • Glandular odotogenic cyst
    • Calcifying epithelial odontogenic cyst (Gorlin cyst)

Odontogenic Tumours

May be true neoplasm or hamartoma, arising from the odontogenic epithelium or ectomesenchyme. Odontogenic lesions tend to lie above the inferior alveolar canal (may displace this inferiorly; cf nonodotogenic lesions). Maxillary lesions tend to be more aggressive than mandibular.

Benign tumours:

  • Ameloblastoma (mandibilar adamantinoma) – Agressive benign lesion. Most mandibular molar, painless (unless infected), M>F. Most multiloculated lytic lesion with scalloped margins, expanded cortex. Solid and cystic components, common mural nodules, marked peripheral enhancement. May have high T1 from haemorrhage or cholesterol. Often associated with dentigerous cyst.
  • Odontoma – Probably a hamartoma with extensive deposition of enamel and dentin.
  • Less common tumours:
    • Calcifying epithelial odontogenic tumour (Pindborg tumour)
    • Squamous odontogenic tumour
    • Odontogenic fibroma – Multiloculated with sclerotic borders, expanded mandible.
    • Odontogenic myxoma
    • Cementoblastoma – <30yo. Circular density attached to mandibular tooth with pencil-thin border, surrounding lucency, radial spicules. Expanded mandible.
    • Mixed odontogenic epithelium and ectomesenchymal tumours – Ameloblastic fibroma/fibro-odontoma/fibrosarcoma, adenomatoid odontogenic tumour, odontoameloblastoma, complex odontoma, compound odontoma

Malignant tumours:

  • Ameloblastic carcinoma
  • Malignant amelobastoma
  • Clear-cell odontogenic carcinoma
  • Ameloblastic fibrosarcoma

Nonodontogenic Lesions

  • Brown tumour – Associated with hyperparathyroidism. Lytic with erosion of lamina dura, ill-defined.
  • Giant cell granuloma – Asymptomatic children and young adults. Well-defined, multilocular with sclerotic borders in mandible.
  • Cherubism – Painless bilateral enlargement of lower face, angelic apperance, AD, regresses after adolescence. Multilocular soap bubble lucencies in posterior mandible, expanded cortex without perforation. DDx fibrous dysplasia.

Squamous Cell Carcinoma (SCC)

(Head and neck SCC, HNSCC). 95% of H&N cancers. Isodense, iso T1, variable T2. Metachronous/synchronous tumours in oral cavity in 40%, other regions is 15%. Lung cancers common, with synchronous primary lung cancers twice as common as lung metastases. Cumulative risk of smoking and alcohol. 50% of cancers harbor HPV (increasing with time), tested by immunuhistochemistry (P16 positive with any H&N HPV strain), HPV16>>HPV18. These cancers tend to start deep in tonsillar crypts (not visible at endoscopy) compared to smoking/EtOH which starts at the epithelium. HPV cancers typically smaller primary with larger nodes, cystic nodes, better prognosis, may metastasize to unusual locations. Other risk factors include nutritional factors, asbestos, irradiation. Sequence of epithelial hyperplasia, atypical hyperplasia, dysplasia, carcinoma in situ to invasive carcinoma.

Recommended baseline CT/MR 8/52 posterior therapy. 90% of recurrences occur in 1st 12 months; patient not considered cured until tumour free for 5yrs. Recurrence at primary site and/or nodes (may be at unusual site as the primary draiange pathway is removed, including dermal drainage being SC stranding/thickening). After radiotherapy tumours tend to occur centrally, at sites of anastomosis, adjacent to surgical clips. Growth of tissue after 8/52, focal exophytic (into extramucusal soft tissue) or endophytic (into lumen) growth. Density, intensity and enhancement characteristics are unreliable. Recurrences best seen on PET.

Nasopharyngeal Carcinoma

Nasopharyngeal malignancies include carcinomas (80%): type 1 is keratinising SCC, 2 nonkeratinising SCC, 3 undifferentiated (lymphoepithelioma) carcinoma (2 and 3 most common); or lymphoma, minor salivary gland tumours or rhabdomyosarocma. Typically small mucosal disease with large submucosal component, may be completely hidden at endoscopy (esp fossa of Rosenmuller). Early peak at 15-25yo (undifferentiated carcinoma) esp Southeast Asia where there is increased risk with EBV (genome incorporated into the carcinoma). Later peak at 50-60yo (squamous and nonkeratinising carcinomas); cumulative risks of smoking and alcohol. Loss of intermuscular fat between levator and tensor veli palatini in the fossa of Rossenmuller. Nodal spread in 80% (even when small), bilateral in 50%, lateral retropharyngeal then level II and V; nodes may be small. Most treated with radiotherapy and chemotherapy with 50-70% 3yr prognosis.

Staging:

  • T1 – Confined to nasopharynx.
  • T2a – Into oropharynx or nasal cavity.
  • T2b – Parapharyngeal extension.
  • T3 – Bones or paranasal sinuses. Require chemoRT.
  • T4 – Intracranial, CNs, infratemporal fossa, hypopharynx, orbit or masticator space.

N2/3 disease require chemoRT.

Surgical contraindication includes tumour encasing ICA or invasion brain/cavernous sinuses. Pterygoid bony invasion below the level of Vidian canal can be resected.

Oropharyngeal SCC

Most commonly anterior tonsil and tongue base (commonly spread past circumvallate papillae). Tonsilllar carcinomas are the most comon carcinoma of unknown primary with cervical adenopathy alone, microscopic involvement deep within the lymphoid tissue crypts invisible to endoscopy and imaging; may invade anterolaterally to retromolar trigone (between maxillary molars and coronoid process), medial to soft palate or anterior to tongue base. Nodal spread in 65%, commonly bilateral to Ib and II.

Features of local invasion:

  • Pre-epiglottic fat – From tongue base into vallucula, may invade pre-epiglottic fat best seen on sagittal and transverse T1. This is impossible to resect while maintaining integrity of the petiole, requiring an epiglottectomy ± laryngectomy.
  • Mandible – Periosteal invasion is almost impossible to see. Cortical invasion shows cortical erosion with enhancement of the defect, low T1 in marrow, tumour on both sides of mandible. Best seen on axial and coronal CT or MR. Marginal cortecectomy (inner cortex resection) performed if tumour is fixed to or invades periosteum or cortex; more extensive mandibular resection if cortex or marrow has been infiltrated.
  • Prevertebral muscles (longus capitus, longus colli) – High T2 with enhancement or nodular infiltration of the muscles, obliteration of retropharyngeal fat stripe suggest invasion but is not very reliable. May require surgical exploration. If involved, tumour is unresectable.
  • Pterygopalatine fossa – May spread along nerves esp CN V to skull base with enlarged enhancing nerves, foraminal enlargement, enhancement in Meckel’s cave, muscular atrophy.
  • Pterygomandibular raphe – Raphe extends from medial pterygoid to mylohyoid ridge of mandible, a site of insertion for buccinator and pharyngeal constrictor. Divides the oral cavity retromolar trigone from oropharynx anterior tonsillar pillar. May extend up to temporalis muscle, pterygomandibular space, floor of mouth or pterygopalatine fossa.
  • Deep invasion of tongue base – If infiltrated bilaterally, limited chance of functioning postsurgical tongue; need at least 25% base of tongue and 1 hypoglossal nerve and 1 lingual a for a functional tongue. Without a functioning tongue, patient requires feeding tube a tracheostomy. Important to determine spread across fatty midline lingual septum (for ?hemiglossectomy). Denervation of tongue causes initial high T2 normal T1 in the hemitongue followed by fatty infiltration high T1 after ~5/12.

Staging:

  • T1 – </= 20mm in greatest dimension.
  • T2 – 20-40mm.
  • T3 – >40mm.
  • T4a – Larynx, deep/extrinsic muscles of tongue, medial patienterygoid, hard palate, mandible.
  • T4b – Lateral pterygoid, pterygoid plates, lateral nasopharynx, skull base, encases carotid a.

Oral Cavity SCC

Increased risk with smoking, alochol, chewing tobacco and betel nuts. Metachronous and synchronous tumours in 40%. Commonly lower lip, floor of mouth, ventral tongue, soft palate, dorsal tongue, gingiva. Best seen on T2 (brighter than dark intrinsic muscles of tongue) and post-T1FS. Floor of mouth tumours may obstruct the submandibular duct with enlarged oedematous gland. Nodal spread 30% at presentation; anterior 2/3 tongue to Ib and II.

Precancerous lesions, increased risk with smoking and chewing tobacco:

  • Leukoplakia – White patch/plaque that cannot be scraped off, without any other diagnosis.
  • Erythroplakia – Red velvety which is less common, but has a higher risk of malignant transformation.

Staging:

  • Tx – Cannot be assessed.
  • T0 – No evidence of primary tumour.
  • Tis – Carcinoma in situ.
  • T1 – </= 20mm in greatest dimension.
  • T2 – 20-40mm.
  • T3 – >40mm.
  • T4 (lip) – Bone, inferior alveolar nerve, floor of mouth, skin of face.
  • T4a (oral cavity) – Bone, deep/extrinsic muscles of tongue, maxillary sinuses, skin of face.
  • T4b – Masticator space, patienterygoid plates, skull base, encases carotid a.

Hypopharyngeal SCC

Often difficult to distinguish hypopharyngeal SCC (lateral piriform sinus) from supraglottic (aryepiglottic fold). The ‘Donald duck’ on transverse images show valleculae (eyes separated by the medial glosso-epiglottic fold) as the lowest limit of the oropharynx), epiglottis, and posterior ‘mouth’ (piriform sinuses). Below this is the ‘flying saucer’ with lateral piriform sinuses (hypopharynx) and anterior fixed portion of the epiglottis; with aryepiglottic folds (supraglottis) between. The hypopharynx is flatted compared to rounded cervical oesophagus; transitions at cricopharyngeus. 60% arise in the piriform sinus (early metastases, aggressive invasion, late presentation), the remainder are postcricoid or posterior pharyngeal. Loss or assymetry of the lateral aspects of the ‘flying saucer’. Prevertebral muscle invasion causes high T2 and enhancement of longus muscles. Nodal spread in 75% at presentation, levels II, III and IV

Staging:

  • T1 – Limited to 1 subsite (postcricoid, piriform sinus, aryepiglottic fold/pharyngeal wall, posterior pharyngeal wall to cricoarytenoid joint), </= 20mm in greatest dimension.
  • T2 – More than 1 subsite or adjacent site, 20-40mm.
  • T3 – >40mm or fixation of hemilarynx.
  • T4a – Thyroid/cricoid cartilage, hyoid, thyroid gland, oesophagus, central comparment of soft tissue (prelaryngeal strap muscles and SC fat).
  • T4b – Prevertebral fascia, encases carotid a, mediastinum.

Supraglottic SCC

May have extensive submucosal glottic and subglottic invasion, appearaing normal at endoscopy. Epiglottic tumours commonly spread to pre-epiglottic fat then petiole and anterior commisure. Aryepiglotic fold and false cord tumours spread to paraglottic fat. All laryngeal carcinomas have a very high rate of nodal spread.

MR is more sensitive but less specific than CT for cartilage invasion. Invasion of ossified cartilage (into bone marrow) is easier than nonossified cartilage. On CT the only absolute finding is erosion with extension into strap muscles. Cartilage sclerosis may be invasion (in 50%) or perichondrial involvement. Arytenoid sclerosis is normal in 16%. On MR cartilage invasion causes high signal on T2FS, enhancement of walls of cartilage.

Staging:

  • T1 – Limited to 1 subsite (false cords, arytenoids, suprahyoid epiglottis, infrahyoid epiglottis, aryepiglottic folds).
  • T2 – More than 1 subsite or outside supraglottis (eg base of tongue, vallecula, medial wall piriform sinus).
  • T3 – Limited to larynx with vocal cord fixation, or invates postcricoid, preepiglottic tissues, paraglottic space, minor thyroid cartilage erosion.
  • T4a – Through thyroid cartilage, tissues beyond larynx (eg trachea, soft tissues of neck, deep extrinsic muscles of tongue, strap muscels, thyroid gland, oesophagus).
  • T4b – Prevertebral space, encases carotid a, mediastinum.

Glottic SCC

Early presentation due to voice changes. Normal glottis at the level of the true cords is tear-drop shape, with anterior commissure </=1mm, and no soft tissue should be on the airway side of the cricoid (posterior commissure). May spread from anterior commissure via neurovascular perforations through thyrohyoid membrane, to paraglottic space or subglottic. Nodal spread less common, unless spreads to supraglottis or subglottis.

Staging:

  • T1a – Limited to 1 vocal cord.
  • T1b – Both vocal cords.
  • T2 – Supraglottic or subglottic, or impaired vocal cord mobility.
  • T3 – Limited to larynx with cord fixation or invates paraglottic spaces, minor thyroid cartilage erosion.
  • T4a – Through thyroid cartilage.

Subglottic SCC

Undersuface of vocal cords and proximal trachea obscured at endoscopy. Usually presents late with poor prognosis. Nodal spread to VI, VII, paratracheal, oesophageal. Subglottic mucosa is very thin, with any nodularity or thickening suspect. There should never be any tissue on the airway side of the cricoid normally.

Staging:

  • T1 – Limited to subglottis.
  • T2 – Vocal cord(s).
  • T3 – Vocal cord fixation.
  • T4a – Cricoid or thyroid cartilage, tissues beyond larynx (eg trachea, soft tissues of neck, deep extrinsic muscles of tongue, strap muscels, thyroid gland, oesophagus).
  • T4b – Prevertebral space, encases carotid a, mediastinum.

Lymphadenopathy

Nodal spread reduces 5-year survival by 50%, bilateral reduces another 50%, extranodal extension (ENE, previously/also termed extracapsular spread ECS) reduces survival by another 50%. Sensitivity for LN and necrosis better on CECT. Nodes >10-15mm maximum short-axis transverse diameter, retropharyngeal nodes >8mm, larger for the jugulodigastric and submandibular nodes. However size is a good indicate for involvement, particular smaller nodes. Suspicious nodes are rounded, necrotic/cystic, heterogneous, clustering, location in typical drainage pathway. Extracapsular spread correlates with size, 25% of <10mm, 75% of >30mm, makes complete local clearance difficult. On power Doppler hilar vessels with branching suggests lymphadenitis whereas peripheral flow suggests metastases. Carotid a invaded if encircled >270deg by tumour.

Nodal stations – See Extracranial Head and Neck (Anatomy)

Cervical lymphadenopathy with no apparant tumour usually occult nasopharyngeal (esp fossa of Rosenmuller), oropharynx (esp tonsils, tongue base, valleculalae), hypopharynx (esp piriform recesses), supraglottic larynx; thyroid, oesophageal, tracheal, bronchial or pulmonary. Primary identified in 25% with CT/MR, improved by additional 25-50% with PET.

Staging for oral cavity, oropharynx, hypopharynx, paranasal sinuses, larynx:

  • Nx – Cannot be assessed.
  • N0 – No regional nodes.
  • N1 – Single ipsilateral node </= 30mm greatest dimension.
  • N2a – Single ipsilateral node 30-60mm.
  • N2b – Multiple ipsilateral nodes.
  • N2c – Bilateral or contralateral nodes.
  • N3 – Any node >60mm.

Staging for nasopharynx:

  • Nx – Cannot be assessed.
  • N0 – No regional nodes.
  • N1 – Unilateral.
  • N2 – Bilateral.
  • N3a – Any nodes >60mm.
  • N3b – Node in supraclavicular fossa.

Metastases staging

  • M0 – No distant metastaes.
  • M1 – Distant metastases.

Treatment

T1-2 cancers usually treated by surgery or TORS (trans-oral robotic surgery). T3-4 cancers usually treated by chemoradiation.

Laryngectomies:

  • Horizontal supraglottic laryngectomy – Incision through plane of ventricle with removal of all structures above including epiglottis, false cords, aryepiglottic foles and pre-epiglottic fat.
  • Vertical hemilaryngectomy (VHL) – Removal of portion of unilateral thyroid cartilage, vocal cord(s) ± arytenoids.
  • Supracricoid laryngectomy – Removal of all thyroid cartilage and epiglottis, usually ipsilateral arytenoid, cricohyoidopexy. If portion of epiglottis is spared then cricohyoidoepiglottopexy.
  • Total laryngectomy.

Neck dissections:

  • Radical neck dissection – Removal of SCM, CNXI, submandibular gland, IJV, level I-V nodes. Minimal residual tissue including skin, aa, anterior viscera.
  • Modified neck dissection – Sparing of SCM, CNXI and/or IJV.
  • Selective neck dissection – Removal of only some nodes.
  • Supramyohyoid dissection – Removal of I-III nodes above cricoid, sparing SCM, IJV and CNXI. Commonly performed for N0 tumours.
  • Anterior dissection – Removal of VI for thyroid cancer.

Reconstruction with flaps/grafts. Auto- (same individual), iso- (identical twin), allo- (same species) or xero- (different species).

  • Grafts bring no native blood supply, relying on supply from surrounding tissues. Fat grafts commonly from abdomen, thigh, flank, breast. Enhancing capsule of parasitised blood vessels.
  • Flaps maintain native blood supply. May be local (rotated), pedicle/regional or free flap/free tissue transfer (from distant site)
  • Tissue –  Single tissue type (eg cutaneous, muscle, bone) or composite (eg myocutaneous)

Radiation will initially cause oedema, increased vascularlity and enhancement to all tissues lasting for weeks, with sequalae of fibrosis. All patients will get some degree of mucositis, some with ulceration (radionecrosis). Radiation associated changes;

  • Salivary/lacrimal glands, tonsils, adenoids – initially oedema and enhancement, later atrophy (fatty atrophy in the glands). In the nasopharynx this will cause a concave ‘U’ shape with loss of normal undulations.
  • Bone marrow – fatty replacement, which in areas of highest dose will persist. Red marrow will return over time in areas receiving less dose.
  • Sinonasal – Sinusitis peaks at 9 months. Granulomatous polyps are exophytic, high T2 with enhancement.
  • Muscles – fibrosis, trismus, dysphagia.
  • Vascular – Accelerated atherosclerosis, which tends to be more diffuse, less calcified, more fibrotic and more rapidly progressive than typical atherosclerosis, also typically sparing the bifurcation, higher risk of re-stenosis. 50% develop carotid stenosis, 1/3 of which have symptoms. Carotid blowout (rare); development of soft tissue/fibrosis around the carotid or exposure to the airway suggests high risk of blowout. Thrombosus. Pseudoaneurysm.
  • Pituitary hypo-function and atrophy
  • Osteoradionecrosis (ORN) of bone or cartilage – Peaks 6-24 months, but can occur at any time. Active phase enhancing mass in marrow, marrow oedema, increased ADC. Inactive phase bone sclerosis, lytic change, fragmentation. PET uptake after 3yrs suggests recurrent tumour.
  • Radiation plexitis can cause enhancement and oedema of nerves. Symptoms include numbess, parasthaesia, limb swelling, weakness. There should be no pain (which is more suspicious of tumour involvement.
  • Brain – Radiation necrosis (typically medial inferior temporal lobes), cysts, abscess. Cranial nerve palsies. WM demyelination, oedema. Micro-/macro-haemorrhages.
  • Radiation associated cancers typically 5-15yrs post treatment, but wide range (can be very delayed with carcinomas). Most are carcinomas (eg SCC), occuring in the low dose field. Sarcomas tend to occur in higher dose field.

Signs or recurrent disease:

  • Convexity along mucosal margins.
  • Enhancement (but less than mucosa), mid-T2 signal (‘evil grey).
  • Mass-like changes >1cm highly suspicious. Changes <1cm should be at least followed up.
  • Increased sclerosis of laryngeal cartilage after RT is suspicious (reduction in sclerosis is good).
  • Persisting diffusion restriction. ADC should increase very quickly after treatment (to suggest response). Change in ADC is a better predictor of response than change in size.
  • PET before 3 months after treatment is unreliable (at 12 weeks 10-15% false positive).